McGill University, Alan Edwards Centre for Research on Pain, Professor, Faculty of Medicine, Department of Anesthesia, and Faculty of Dentistry
Luda Diatchenko, MD, PhD is a Canada Excellence Research Chair in Human Pain Genetics, Professor, Faculty of Medicine, Department of Anesthesia, and Faculty of Dentistry, at McGill University, Alan Edwards Centre for Research on Pain. She earned her MD and PhD in the field of Molecular Biology from the Russian State Medical University. Dr. Diatchenko started her career in industry, she was a Leader of the RNA Expression Group at Clontech, Inc., and subsequently, Director of Gene Discovery at Attagene, Inc. During this time, Dr. Diatchenko was actively involved in the development of several widely-used and widely-cited molecular tools for the analysis of gene expression and regulation.
Dr. Diatchenko’s academic career started at 2000 in the Center for Neurosensory Disorders at the University of North Carolina. Her research since then is focused on determining the cellular and molecular biological mechanisms by which functional genetic variations impact human pain perception and risk of development of chronic pain conditions, enabling new approaches to identify new drug targets, treatment responses to analgesics, and diagnostic. Multiple collaborative activities allow the Diatchenko group to take basic genetic findings all the way from human association studies, through molecular and cellular mechanisms, to animal models, and ultimately to human clinical trials.
In total, Dr. Diatchenko have authored or co-authored over 100 peer-reviewed research papers (plus 10 book chapters) in journals with 2011 Thomson ISI Impact Factors up to 34.8, from which 34 (44%) of refereed articles in journals having an Impact Factor >5.0.
Current research
Persistent pain is a part of many common human clinical conditions, yet the current ability to diagnose and manage these conditions is inadequate. Pain perception is one of the most complicated measurable traits, as it is composed of an aggregate of several other measurable phenotypes associated with peripheral and central nervous system dynamics, stress responsiveness, and inflammatory state. It is generally accepted that complex traits, like pain perception, result from the interplay between environmental exposures and multiple genetic variants. However, little is known about the nature of these genetic variants. Because of the established roles of environmental exposures and the commonly held view that pain perception is an unquantifiable “subjective” experience, a genetic basis for pain perception has long been questioned. Recent and rapidly developing discoveries in the field of pain genetics have provided evidence for a substantial role for genetic background on pain perception and clinical pain phenotypes. These findings provide unique opportunities to identify new genetic variants that contribute to pain phenotypes.
The Diatchenko lab investigates the psychological, molecular, cellular, and genetic pathways that mediate both acute and persistent pain states. Their primary goal is to identify the critical elements of human genetic variability contributing to pain sensitivity and pathophysiological pain states that will enable individualized treatments and therapies. Other related research endeavors include molecular hierarchy of functional SNPs (single-nucleotide polymorphisms) and SNP-depend regulation of gene expression, underlying molecular pain signaling. Answering these questions requires collaboration with experts in both clinical and basic biological sciences. Such collaborative activities allow the Diatchenko group to take basic genetic findings all the way from human association studies, through molecular and cellular mechanisms, to animal models, and ultimately to human clinical trials.
Projects
1. Functional molecular genetic analysis of the Association Studies results of human chronic pain conditions.
2. Assessment of enzymatic activity of COMT homologs.
3. Study on genotype dependent variation within COMT gene locus in post-surgical opioid-induced analgesia.